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Biomedical subjects

C Saunier

Publications and source records attributed to C Saunier.

At least 55 records · Page 3Linked to original sources
PubMed1985

Cimetidine inhibits the hypoxia-induced increase in cerebral blood flow in dogs.

Cimetidine is an H2 receptor-blocking drug frequently given to ICU patients for the prevention of stress ulcers. However, histamine causes potent cerebral vasodilation through the H2 receptors. This study tested the hypothesis that cimetidine, by blocking the H2 receptors, could blunt the increase of cerebral blood flow induced by hypoxia. We induced isocapnic hypoxia in 12 conscious dogs that were randomly divided into two groups. Six dogs received no treatment (control group), and the other six received iv cimetidine (4 mg/kg) to block the H2 receptors. Cerebral blood flow (CBF) was measured with the radioactive microsphere technique before, and 2 and 4 h after hypoxia was induced. In the control group, CBF significantly increased with hypoxia in all the regions of the brain. Cimetidine blunted this increase in all the regions of the brain except the pons and bulb. As a result of the reduced flow, cimetidine significantly decreased the oxygen supply to the brain compared to the control group. We conclude that cimetidine blunts the increase in CBF during hypoxia and might reduce oxygen supply to the brain in hypoxic patients.

Animals↗
PubMed1985

Influence of hypoxemia and respiratory acidosis on the plasma kinetics and tissue distribution of digoxin in the conscious dog.

The aim of the present study was to investigate the influence of hypoxemia combined with respiratory acidosis on the kinetics of digoxin in conscious dogs. One group of three beagles was exposed to air and 7 days later to 10% O2, 10% CO2, and 80% N2. In a second group of three dogs, the order of exposure to the two atmospheric conditions was reversed. The dogs received 25 micrograms/kg digoxin and blood and urine samples were collected over the next 29 h. At the conclusion of the second treatment, the dogs were sacrificed to determine digoxin concentrations in the left ventricle, liver, renal cortex, and skeletal muscle. Digoxin total body clearance increased from 6.2 +/- 0.9 in control to 9.0 +/- 1.0 mL X min-1 X kg-1 in hypoxemic and hypercapnic dogs (p less than 0.05). The digoxin apparent volume of distribution at steady state (Vss) was increased in the dogs with hypoxemia and hypercapnia (11.63 +/- 1.11 vs. 8.62 +/- 0.41 L/kg in the controls, p less than 0.05). As a consequence the digoxin plasma half-life remained unchanged (18.6 +/- 1.5 h in hypoxemic and hypercapnic dogs versus 20.1 +/- 2.8 h in the controls). In dogs with hypoxemia and hypercapnia, the ratio of tissue to plasma digoxin concentrations tended to increase in the liver, in the renal cortex, and in the left ventricle and remained unchanged in the left hind leg muscle. In vitro studies showed that the digoxin total binding to erythrocyte membranes was slightly increased in the dogs with hypoxemia and hypercapnia, resulting from an increase in the apparent intrinsic association constant for digoxin (p less than 0.003). It is concluded that hypoxemia combined with respiratory acidosis changes digoxin disposition in the conscious dog and is the cause of a digoxin redistribution into the tissues.

Acidosis, Respiratory↗
PubMed1985

In vitro effects of hypoxia and (or) hypercapnic acidosis on the myocardial uptake of digoxin.

A recent study has shown in the conscious dog that hypoxia associated with respiratory acidosis could increase the in vivo distribution of digoxin in the myocardium. The aim of the present study was to evaluate in vitro the effects of hypoxia and (or) hypercapnic acidosis on the digoxin uptake. For this purpose, rat myocardium was incubated for 180 min with radiolabelled [3H]digoxin. The uptake of digoxin which was expressed in nanograms of digoxin bound per 100 mg of myocardium was decreased by hypoxia and increased by hypercapnic acidosis. The association of hypoxia and hypercapnic acidosis had no effect on the digoxin uptake, suggesting that in vitro hypoxia acts in an opposite way to hypercapnia.

Acidosis↗
PubMed1985

The influence of hypoxemia on tritiated digoxin plasma kinetics and tissue distribution in the conscious dog.

The goals of this study were to document the effect of hypoxemia on the distribution of digoxin in conscious dogs. For this purpose, 6 beagles were exposed to air and 6 others to an atmosphere containing 10% O2, to generate a PaO2 equal to 46.3 +/- 0.3 mmHg (mean +/- SEM). The animals received 25 micrograms/kg of digoxin containing 2.17 micrograms/kg of 3H-digoxin, and then blood and urine samples were collected over the next 48 h, at which time they were killed to determine digoxin concentrations in several tissues. Five additional beagles were used to assess the influence of hypoxemia on the blood perfusion to these tissues using radioactive microspheres. The results, expressed as digoxin equivalents, indicated that hypoxemia increased the digoxin apparent volume of distribution (2.85 +/- 0.10 versus 2.01 +/- 0.11 L/kg; p less than 0.001) and the time required to achieve this distribution (9.7 +/- 1.4 versus 2.6 +/- 0.3 h; p less than 0.01). As digoxin clearance was not influenced by hypoxemia, the half-life was increased from 25.2 +/- 1.5 to 33.4 +/- 1.3 h (p less than 0.01). With hypoxemia, digoxin concentrations increased significantly in the brain and diaphragmatic muscle, but only marginally in other organs, including the heart, the latter despite a significant increase in blood flow. It is concluded that hypoxia does change digoxin disposition but does not increase digoxin heart concentrations. Therefore, factors other than changes in digoxin plasma kinetics and heart distribution may be responsible for the decrease in digitalis tolerance during hypoxemia.

Animals↗
PubMed1984

Papain-induced emphysema: the influence of preliminary oxygenation.

Rats were exposed for 7 days to an oxygen concentration of 85% and then submitted to an aerosol of papain, immediately, 3, 7 or 15 days after this exposure. The number of animals dying increased as the time between the administration of papain and the end of the exposure to oxygen increased. The quantification of emphysema was made by measurement of the mean linear intercept (LM). The LM does not differ between animals pretreated with oxygen and which have received papain, immediately or after 3 days, and the controls in air not having received papain. On the contrary, the animals pretreated with oxygen and having received papain 7 or 15 days later show a significantly higher LM than do the controls in air having received papain. The protection of the lung against the elastolytic effect of papain by a preliminary stay in 85% O2 is short-term; its mechanism is discussed.

Animals↗
PubMed1982

Square-wave endurance exercise test (SWEET) for training and assessment in trained and untrained subjects. II. Blood gases and acid-base balance.

In order to obtain information about physiological and homeostasic responses at the maximal Intensity of Endurance of the 45 min "Square-Wave Endurance Exercise Test" (MIE45), three arterial blood samples were taken: (a) at rest; (b) at the 45th min of the SWEET; (c) after 15 min of recovery, to measure paO2, paCO2, [H+], [Hb], and [lactate] in 14 normal male subjects: four trained (T) six well trained (WT) and four others untrained (U). Total mechanical work (TMW) corresponding to MIE45 was significantly higher (mean +/- SEM) respectively in WT (9.22 +/- 0.65 kJ . kg-1, p less than 0.001), than in T (7.17 +/- 0.18 kJ . kg-1, p less than 0.01) and U subjects (4.44 +/- 0.36, p less than 0.001). Because of this the lactate level, which rose significantly during exercise, differed between U and WT subjects (p less than 0.05). In spite of the exhaustive character of the MIE45, [H+] and paO2 remained within the range of normal values. These results suggest that trained and untrained subjects can be trained with the exhausting MIE45 exercise while maintaining a constant [H+] and paO2 at the 45th min of exercise.

Acid-Base Equilibrium↗
PubMed1981

Respiratory acidemia and theophylline pharmacokinetics in the awake dog.

Recently, respiratory acidemia has been shown to be associated with an altered volume of distribution (Vd) of theophylline in patients during an acute exacerbation of chronic obstructive pulmonary disease. However, many factors other than acidemia could have altered the pharmacokinetics. Our purpose was to study the effects of respiratory acidemia alone. Six awake dogs had normocapnia and hypercapnia induced in a conditioned chamber. After intravenous injection (8 mg/kg), plasma theophylline concentrations were measured for 8 hours by means of quantitative enzyme immunoassay technique. There were no statistically significant effects of respiratory acidosis on Vd and total theophylline clearance. There was no significant correlation between these variables and pH, PCO2, PO2. We conclude that respiratory acidosis, per se, does not effect theophylline pharmacokinetics in dogs.

Acidosis, Respiratory↗
PubMed1980

Pentose pathway in pulmonary fibrosis due to chronic paraquat poisoning.

In 14 beagle dogs, paraquat was infused in fractional doses to produce pulmonary fibrosis while avoiding fatal liver and kidney lesions. Activity of the three enzymes of the pentose pathway: glucose-6-phosphate dehydrogenase (G-6-PDH), glutathione reductase (GR) and glutathione peroxidase (GSH Px), which supply reduced equivalents against oxidant agents, were measured in the mediastinal lobe of the lung. After a single low dose (2-3 mg/kg body weight), GR and GSH Px activities were reduced. After repeated paraquat doses, pentose pathway enzyme activities were higher than after a single low dose; however, they did not significantly exceed the normal values as determined in control dogs. The activities of G-6-PDH, GR and GSH Px correlated with the total paraquat dose and with the extent of pulmonary fibrosis measured with an electronic image analyzer. The activity of pulmonary lactate dehydrogenase, which was also reduced after a single low dose of paraquat, did not show the same correlations.

Animals↗
PubMed1977

Post-hypercapnia recovery in the dog: arterial blood acid-base equilibrium and glycolysis.

Changes in acid-base equilibrium and blood lactate and pyruvate concentrations were studied during recovery (breathing room air) after three days hypercapnia (FICO2 = 0.10) in awake dogs. Fast return to FICO2 = 0 produced a slight alkalosis in arterial blood and an increase in lactate and pyruvate concentrations which seemed to be maximum at the 15th minute. These changes were inhibited by previous injection of acetazolamide (50 mg/kg body weight). During progressive return to FICO2 = 0, over 1 hour, the peak value of blood lactate and pyruvate was delayed until the end of that hour, at the same time as a slight blood alkalosis appeared. These phenomen are most probably explained by a stimulation, due to alkalosis, of glycolysis at the level of phosphofructokinase.

Acetazolamide↗